Lateralization of epileptiform discharges in patients with epilepsy and precocious destructive brain insults

Unilateral destructive brain lesions of early development can result in compensatory thickening of the ipsilateral cranial vault. The aim of this study was to determine the frequency of these bone changes among patients with epilepsy and precocious destructive lesions, and whether a relationship exists between these changes and epileptiform discharges lateralization. Fifty-one patients had their ictal/inter-ictal scalp EEG and skull thickness symmetry on MRI analyzed. Patients were divided into three main groups according to the topographic distribution of the lesion on the MRI: hemispheric (H) (n=9); main arterial territory (AT) (n=25); arterial borderzone (Bdz) (n=17). The EEG background activity was abnormal in 26 patients and were more frequent among patients of group H (p=0.044). Thickening of the skull was more frequent among patients of group H (p=0.004). Five patients (9.8%) showed discordant lateralization between epileptiform discharges and structural lesion (four of them with an abnormal background, and only two of them with skull changes). in one of these patients, ictal SPECT provided strong evidence for scalp EEG false lateralization. The findings suggest that compensatory skull thickening in patients with precocious destructive brain insults are more frequent among patients with unilateral and large lesions. However, EEG lateralization discordance among these patients seems to be more related to EEG background abnormalities and extent of cerebral damage than to skull changes.6211

Variation of nuclear areas of bull spermatozoa subjected to feulgens reaction

sem informação1911

VARIATION OF NUCLEAR AREAS OF BULL SPERMATOZOA SUBJECTED TO FEULGENS REACTION

1911

FEULGEN-DNA PLUG AND 2-WAVELENGTH CYTOPHOTOMETRY OF BULL SPERMATOZOA

324179512913

Cerebral atrophy related to corticotherapy in systemic lupus erythematosus (SLE)

The aim of this study was to evaluate the frequency and intensity of cerebral atrophy using CT scanning and the possible relation to corticosteroid therapy or disease in systemic lupus erythematosus (SLE) and to analyse the relationships between cerebral atrophy and activity disease and neuropsychiatric manifestations in lupus patients. We studied 107 consecutive SLE patients (American Rheumatology Association 1982 criteria) who were taking steroid drugs at the time and not selected for any particular manifestation (group 1). A complete clinical, neurological and laboratory evaluation was performed. The American College of Rheumatology's classification for neuropsychiatric manifestations and SLE disease activity index for activity were employed. Group 2 comprised 39 non-SLE patients with oral chronic steroid use (I mg/k/day for more than 3 consecutive months); 50 normal individuals were the controls (group 3). There were no demographic differences between the groups. Brain CT was performed in all individuals and the frequency and the intensity (minimal, moderate and severe) of atrophy analysed, through well-defined measures and indices, by two neuroradiologists. Cerebral atrophy was significantly more frequent in groups I and 2 than in group 3, but with no significant difference between groups I and 2. The severity of cerebral atrophy was significantly higher in SLE patients (p <0.05), independent of steroid dose or duration of disease. In both groups no patient presented severe atrophy. Lupus patients with and without cerebral atrophy presented neuropsychiatric manifestations and activity disease in a similar proportion. The more frequent neuropsychiatric manifestation in lupus patients with cerebral atrophy was seizures (p <0.05). Chronic glucocorticoid therapy was responsible for cerebral atrophy, with a comparable incidence in both lupus and non-lupus patients compared to age and gender-matched normal subjects untreated with glucocorticoids. The disease activity was not related to cerebral atrophy in group I and seizures were the neurologic manifestation related to cerebral atrophy. The severity of the cerebral atrophy was independent of steroid dose, or duration of treatment. Moreover, the disease itself contributes to the severity of this process, but not to the development of cerebral atrophy.20424525

Proton magnetic resonance spectroscopy and magnetic resonance imaging findings in a patient with central nervous system paracoccidioidomycosis

The authors describe a patient with brain paracoccidioidomycosis whose magnetic resonance image (MRI) showed multiple hypointense lesions on T2-weighted images with peripheral enhancement after gadolinium injection. Single-voxel proton magnetic resonance spectroscopy (H-MRS) of one of the lesions showed 2 peaks at 0.9 and 1.32 ppm, corresponding to lipid signals, indicating intense necrosis. The other characteristic peaks of H-1-MRS were undifferentiated from baseline. These findings, although not specific, may help to differentiate fungal abscess from tumoral lesions and other types of abscess.14437737

Lipidized giant-cell glioblastoma of cerebellum

Glioblastoma multiforme is recognized rarely in the cerebellum. We describe a peculiar case with lipid accumulation in giant tumor cells, possibly the second example so far reported in this unusual location. A 46-year-old man with a 5-month history of headache, vomiting, dizziness and instability of gait, was found to have on magnetic resonance imaging an expanding mass situated deep in the left cerebellar hemisphere. The lesion was hypointense in T1 - and hyperintense in T2-weighted images, had poorly defined borders, peripheral edema and annular foci of contrast enhancement. Eight months after subtotal removal and radiotherapy, control MRI showed tumor recurrence with aggressive features. The patient was alive 15 months after operation but follow-up was eventually lost. Histologically, the tumor showed marked pleomorphism, with many giant cells characterized by finely vacuolated cytoplasm strongly suggestive of lipid accumulation. There were few, sometimes atypical mitotic figures and foci of endothelial proliferation. The tumor cells were strongly positive for GFAP, vimentin and S100 protein, all of which stressed the foamy appearance of the giant cells. About 15% of nuclei were positive for Ki-67. We considered the case to be a so-called lipidized glioblastoma, first recognized as a subtype by Kepes and Rubinstein [198 1]. Differential diagnosis with anaplastic pleomorphic xanthoastrocytoma is discussed.24626226

Brainstem Involvement in Sjogren's Syndrome-Related Sensory Neuronopathy

BACKGROUND AND PURPOSE Sensory neuronopathies (SN) are peripheral nervous system disorders associated with degeneration of dorsal root ganglion neurons. Magnetic resonance imaging (MRI) studies have shown abnormalities limited to T2-weighted high signal intensity in the posterior columns. METHODS AND RESULTS A 65-year-old woman with Sjogren syndrome had slowly progressive unsteadiness of gait and limb paresthesias. A blink reflex examination suggested a paramedian brainstem lesion, confirmed by MRI. CONCLUSIONS Sjogren's syndrome-related SN may be associated with a more diffuse immune-mediated aggression, involving also the brainstem, and leading to some of the blink reflex abnormalities observed in nonparaneoplastic SN.20439739

Dissemination patterns of pilocytic astrocytoma

Two patients with multifocal pilocytic astrocytoma diagnosed by magnetic resonance imaging (MRI) and confirmed by histopathological examination are reported. They presented distinct sites and mechanisms of metastasis: to distant ventricles through the cerebral spinal fluid (CSF) in patient 1 and to contralateral parenchyma, possibly through white matter tracts, in patient 2, a pathway not so far reported in pilocytic astrocytoma. Early detection of multifocal pilocytic astrocytoma by MRI may change treatment strategies and improve prognosis. (c) 2005 Elsevier B.V. All rights reserved.108656857

Epilepsy and destructive brain insults in early life: a topographical classification on the basis of MRI findings

Destructive insults of early development can lead to a wide variety of lesional patterns and are a wet[ known cause of epilepsy. The aim of this study is to present a topographic magnetic resonance imaging (MRI) classification of these lesions in adult patients with epilepsy. Thirty-three consecutive patients were divided in three groups according to the topographic distribution of their Lesion on MRI: hemispheric (H, n = 7); main arterial territory (AT, n = 18); arterial borderzone (Bdz, n = 8). We analyzed clinical, MRI and magnetic resonance angiography (MRA) data. Status epilepticus (SE) during childhood was more common in group H (7/7) than in the groups AT (1/18) and Bdz (0/8) (P < 0.001). MRA pattern of impaired flow signal in the distal segments of at[ three major arteries in the affected hemisphere was present in 85.7% of group H patients, and was exclusive to this group. 88.8% (16/18) of patients from group AT presented congenital motor deficit, in contrast to 37.5% (3/8) of group Bdz, and in none of group H (P < 0.001). All patients with Bdz Lesions had antecedent of fetal distress, in contrast to 1/7 from group H and 5/18 of group AT (P = 0.001). The MRAs of patients with Bdz lesions were often normal except in those with larger lesions. Our data suggest that in adult patients with epilepsy due to precocious destructive brain insults, a MRI topographical classification distributes them in relatively homogenous clinical groups. (C) 2003 BEA Treading Ltd. Published by Elsevier Ltd. All rights reserved.13638339